The roles and mechanisms of PAR4 and P2Y12/phosphatidylinositol 3‐kinase pathway in maintaining thrombin‐induced platelet aggregation

BACKGROUND AND PURPOSE Activation of human platelets by thrombin is mediated predominately through two proteinase‐activated receptors (PARs), PAR1 and PAR4. Phosphatidylinositol 3‐kinase (PI3K) inhibition leads to reversible PAR1‐mediated platelet aggregation, but has no effect on the stability of platelet aggregation induced by thrombin. In the present study, the molecular mechanisms underlying this difference were investigated.

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